Bcl-2 Increases Memory B Cell Recruitment but Does Not Perturb Selection in Germinal Centers

Immunity. 1994 Dec;1(9):803-13. doi: 10.1016/s1074-7613(94)80022-7.


To address the role of apoptosis in the humoral immune response, we have examined a well-characterized T cell-dependent B cell response in mice expressing transgenic Bcl-2 in their B lymphocytes. The selection of somatic mutants and the appearance of high affinity antibodies was not affected by constitutive Bcl-2 expression. Such expression did, however, disproportionately increase the antigen-specific memory B cell pool, suggesting that the final size of the memory compartment may be regulated by an apoptotic process, which, in turn, can be influenced by Bcl-2. In addition, transgenic mice showed prolonged survival of foci of early antibody-producing cells, suggesting their removal is mediated by apoptosis that can be blocked by Bcl-2.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / immunology
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • Base Sequence
  • Humans
  • Immunity
  • Immunologic Memory
  • Mice
  • Mice, Transgenic
  • Molecular Sequence Data
  • Proto-Oncogene Proteins / immunology*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2
  • Spleen / immunology
  • Spleen / pathology


  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2